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Article ; Online: Acylglycine Analysis by Ultra-Performance Liquid Chromatography-Tandem Mass Spectrometry (UPLC-MS/MS).

Hobert, Judith A / Guymon, Rebecca / Yuzyuk, Tatiana / Pasquali, Marzia

Current protocols

2023 Volume 3, Issue 4, Page(s) e758

Abstract: Quantitative analysis of urine acylglycines has shown to be a highly sensitive and specific method with proven clinical utility for the diagnosis of several inherited metabolic disorders including: medium chain acyl-CoA dehydrogenase deficiency, multiple ...

Abstract	Quantitative analysis of urine acylglycines has shown to be a highly sensitive and specific method with proven clinical utility for the diagnosis of several inherited metabolic disorders including: medium chain acyl-CoA dehydrogenase deficiency, multiple acyl-CoA dehydrogenase deficiency, short chain acyl-CoA dehydrogenase deficiency, 3-methylcrotonyl-CoA carboxylase deficiency, 2-methylbutyryl-CoA dehydrogenase deficiency, isovaleric acidemia, propionic academia, and isobutyryl-CoA dehydrogenase deficiency. Here, a method that is currently performed using ultra-performance liquid chromatography/tandem mass spectrometry (UPLC-MS/MS) is described. © 2023 Wiley Periodicals LLC. Basic Protocol: Urinary acylglycine analysis by UPLC-MS/MS Support Protocol 1: Quality control preparation Support Protocol 2: Internal standard (ISTD) preparation Support Protocol 3: Standard (STD)/calibrator preparation.
MeSH term(s)	Humans ; Chromatography, Liquid/methods ; Tandem Mass Spectrometry/methods ; Chromatography, High Pressure Liquid/methods ; Amino Acid Metabolism, Inborn Errors/diagnosis ; Glycine
Chemical Substances	Glycine (TE7660XO1C)
Language	English
Publishing date	2023-04-28
Publishing country	United States
Document type	Journal Article
ISSN	2691-1299
ISSN (online)	2691-1299
DOI	10.1002/cpz1.758
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Article ; Online: Quantitation of Butyrylcarnitine, Isobutyrylcarnitine, and Glutarylcarnitine in Urine Using Ultra-Performance Liquid Chromatography-Tandem Mass Spectrometry (UPLC-MS/MS).

Hobert, Judith A / Brose, Stephen A / Pasquali, Marzia

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2546, Page(s) 83–94

Abstract: Acylcarnitines are formed when an acyl group is transferred from coenzyme A to a molecule of L-carnitine. In organic acidemias, and in fatty acid oxidation disorders, specific acylcarnitine species accumulate in a pattern that is characteristic for each ... ...

Abstract	Acylcarnitines are formed when an acyl group is transferred from coenzyme A to a molecule of L-carnitine. In organic acidemias, and in fatty acid oxidation disorders, specific acylcarnitine species accumulate in a pattern that is characteristic for each disease. For this reason, acylcarnitine analysis is widely used for screening and diagnosis of inherited disorders of metabolism. The most common method for acylcarnitine analysis uses flow injection tandem mass spectrometry. Flow injection analysis allows for high throughput, however, does not provide separation of isomeric and isobaric compounds. Among the acylcarnitine species which can be affected by the presence of isomeric/isobaric compounds, C4-carnitine and C5DC-carnitine are probably the ones encountered most often. The method presented here is performed on urine and utilizes butanolic HCL to derivatize acylcarnitines, ultra-performance liquid chromatography to resolve C4- and C5-DC isomers and isobars, and quantitation of these species using multiple-reaction monitoring (MRM).
MeSH term(s)	Carnitine/analogs & derivatives ; Carnitine/analysis ; Chromatography, High Pressure Liquid/methods ; Chromatography, Liquid/methods ; Coenzyme A ; Fatty Acids ; Tandem Mass Spectrometry/methods
Chemical Substances	Fatty Acids ; acylcarnitine ; glutarylcarnitine (109006-11-3) ; isobutyryl-1-carnitine (25518-49-4) ; butyrylcarnitine (25576-40-3) ; Carnitine (S7UI8SM58A) ; Coenzyme A (SAA04E81UX)
Language	English
Publishing date	2022-09-20
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2565-1_8
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Article ; Online: Diagnosing X-Linked Adrenoleukodystrophy after Implementation of Newborn Screening: A Reference Laboratory Perspective.

Prinzi, Julia / Pasquali, Marzia / Hobert, Judith A / Palmquist, Rachel / Wong, Kristen N / Francis, Stephanie / De Biase, Irene

International journal of neonatal screening

2023 Volume 9, Issue 4

Abstract: Adrenoleukodystrophy (ALD) is caused by pathogenic variants in ... ...

Abstract	Adrenoleukodystrophy (ALD) is caused by pathogenic variants in the
Language	English
Publishing date	2023-11-02
Publishing country	Switzerland
Document type	Journal Article
ISSN	2409-515X
ISSN (online)	2409-515X
DOI	10.3390/ijns9040064
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Article ; Online: Quantitative analysis of urine acylglycines by ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS): Reference intervals and disease specific patterns in individuals with organic acidemias and fatty acid oxidation disorders.

Hobert, Judith A / De Biase, Irene / Yuzyuk, Tatiana / Pasquali, Marzia

Clinica chimica acta; international journal of clinical chemistry

2021 Volume 523, Page(s) 285–289

Abstract: Background: Acylglycine species accumulate in specific disorders of branched-chain amino acid metabolism and fatty acid β-oxidation. These species are excreted in urine and their analysis can facilitate diagnosis. Previous studies evaluated reference ... ...

Abstract	Background: Acylglycine species accumulate in specific disorders of branched-chain amino acid metabolism and fatty acid β-oxidation. These species are excreted in urine and their analysis can facilitate diagnosis. Previous studies evaluated reference ranges and increases in metabolic patients, but these involved small numbers of individuals. We have conducted an analysis encompassing large numbers of individuals to better characterize the reference ranges of these analytes and additionally describe our findings from patients with confirmed metabolic disorders. Methods: We conducted a retrospective analysis of approximately 9 y of urine acylglycine data from our clinical laboratory. Acylglycines were extracted from urine, derivatized and analyzed using UPLC-MS/MS. Reference ranges were determined from the non-diseased population. Data from confirmed patients were used to document the range of increases observed in these conditions and to generate multiple of the median graphs. Results: In total, 6162 urine specimens from 5633 patients with and without metabolic disorders were analyzed. Magnitude and pattern of acylglycine elevations in patients with confirmed metabolic disorders were documented. Conclusion: This manuscript extends our previously published method by providing the reference ranges and disease specific elevations and patterns of urine acylglycine species using the largest data set published to date.
MeSH term(s)	Chromatography, High Pressure Liquid ; Chromatography, Liquid ; Fatty Acids ; Humans ; Laboratories, Clinical ; Lipid Metabolism, Inborn Errors ; Reference Values ; Retrospective Studies ; Tandem Mass Spectrometry
Chemical Substances	Fatty Acids
Language	English
Publishing date	2021-10-08
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80228-1
ISSN	1873-3492 ; 0009-8981
ISSN (online)	1873-3492
ISSN	0009-8981
DOI	10.1016/j.cca.2021.10.007
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Article ; Online: Phenylalanine hydroxylase deficiency treatment and management: A systematic evidence review of the American College of Medical Genetics and Genomics (ACMG).

Adams, April D / Fiesco-Roa, Moisés Ó / Wong, Lawrence / Jenkins, Gabrielle P / Malinowski, Jennifer / Demarest, Olivia M / Rothberg, Paul G / Hobert, Judith A

Genetics in medicine : official journal of the American College of Medical Genetics

2023 Volume 25, Issue 9, Page(s) 100358

Abstract: Purpose: Elevated serum phenylalanine (Phe) levels due to biallelic pathogenic variants in phenylalanine hydroxylase (PAH) may cause neurodevelopmental disorders or birth defects from maternal phenylketonuria. New Phe reduction treatments have been ... ...

Abstract	Purpose: Elevated serum phenylalanine (Phe) levels due to biallelic pathogenic variants in phenylalanine hydroxylase (PAH) may cause neurodevelopmental disorders or birth defects from maternal phenylketonuria. New Phe reduction treatments have been approved in the last decade, but uncertainty on the optimal lifespan goal Phe levels for patients with PAH deficiency remains. Methods: We searched Medline and Embase for evidence of treatment concerning PAH deficiency up to September 28, 2021. Risk of bias was evaluated based on study design. Random-effects meta-analyses were performed to compare IQ, gestational outcomes, and offspring outcomes based on Phe ≤ 360 μmol/L vs > 360 μmol/L and reported as odds ratio and 95% CI. Remaining results were narratively synthesized. Results: A total of 350 studies were included. Risk of bias was moderate. Lower Phe was consistently associated with better outcomes. Achieving Phe ≤ 360 μmol/L before conception substantially lowered the risk of negative effect to offspring in pregnant individuals (odds ratio = 0.07, 95% CI = 0.04-0.14; P < .0001). Adverse events due to pharmacologic treatment were common, but medication reduced Phe levels, enabling dietary liberalization. Conclusions: Reduction of Phe levels to ≤360 μmol/L through diet or medication represents effective interventions to treat PAH deficiency.
MeSH term(s)	Pregnancy ; Female ; Humans ; United States ; Genetics, Medical ; Phenylalanine ; Phenylketonurias/drug therapy ; Phenylketonurias/genetics ; Phenylalanine Hydroxylase/genetics ; Phenylketonuria, Maternal ; Genomics
Chemical Substances	Phenylalanine (47E5O17Y3R) ; Phenylalanine Hydroxylase (EC 1.14.16.1)
Language	English
Publishing date	2023-07-20
Publishing country	United States
Document type	Systematic Review ; Practice Guideline ; Journal Article
ZDB-ID	1455352-1
ISSN	1530-0366 ; 1098-3600
ISSN (online)	1530-0366
ISSN	1098-3600
DOI	10.1016/j.gim.2022.12.005
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Article ; Online: Acylglycine Analysis by Ultra-Performance Liquid Chromatography-Tandem Mass Spectrometry (UPLC-MS/MS).

Hobert, Judith A / Liu, Aiping / Pasquali, Marzia

Current protocols in human genetics

2016 Volume 91, Page(s) 17.25.1–17.25.12

Abstract	Quantitative analysis of urine acylglycines has shown to be a highly sensitive and specific method with proven clinical utility for the diagnosis of several inherited metabolic disorders including: medium chain acyl-CoA dehydrogenase deficiency, multiple acyl-CoA dehydrogenase deficiency, short chain acyl-CoA dehydrogenase deficiency, 3-methylcrotonyl-CoA carboxylase deficiency, 2-methylbutyryl-CoA dehydrogenase deficiency, isovaleric acidemia, propionic academia, and isobutyryl-CoA dehydrogenase deficiency. Here, a method that is currently performed using ultra-performance liquid chromatography/tandem mass spectrometry (UPLC-MS/MS) is described. © 2016 by John Wiley & Sons, Inc.
MeSH term(s)	Amino Acid Metabolism, Inborn Errors/diagnosis ; Amino Acid Metabolism, Inborn Errors/urine ; Chromatography, Liquid/methods ; Glycine/analogs & derivatives ; Glycine/urine ; Humans ; Tandem Mass Spectrometry/methods
Chemical Substances	N-acylglycine esters ; Glycine (TE7660XO1C)
Language	English
Publishing date	2016-10-11
Publishing country	United States
Document type	Journal Article
ISSN	1934-8258
ISSN (online)	1934-8258
DOI	10.1002/cphg.19
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Article: Extrapolation of Variant Phase in Mitochondrial Short-Chain Enoyl-CoA Hydratase (ECHS1) Deficiency.

Carlston, Colleen M / Ferdinandusse, Sacha / Hobert, Judith A / Mao, Rong / Longo, Nicola

JIMD reports

2018 Volume 43, Page(s) 103–109

Abstract: Loss-of-function and hypomorphic ECHS1 variants are associated with mitochondrial short-chain enoyl-CoA hydratase deficiency, an inborn error of valine metabolism. We report an 8-year-old boy with developmental delay, ataxia, hemiplegia, and hearing loss ...

Abstract	Loss-of-function and hypomorphic ECHS1 variants are associated with mitochondrial short-chain enoyl-CoA hydratase deficiency, an inborn error of valine metabolism. We report an 8-year-old boy with developmental delay, ataxia, hemiplegia, and hearing loss with abnormalities in the basal ganglia. Biochemical studies were essentially normal except for a persistent mildly elevated CSF alanine. This patient demonstrates an intermediate phenotype between a Leigh-like, early-onset presentation and paroxysmal exercise-induced dyskinesia. Two novel ECHS1 variants (c.79T>G; p.Phe27Val and c.789_790del; p.Phe263fs) were identified via exome sequencing in the proband, and pathogenicity was confirmed by enzyme assay performed on patient fibroblasts. Neither of the ECHS1 variants detected in the child were present in the mother. However, due to nearby polymorphisms, it was possible to determine that p.Phe263fs occurred de novo on the maternal chromosome and that p.Phe27Val likely derived from the paternal chromosome. Nearby polymorphisms can help set phase of variants when only a single parent is available for testing or when an identified variant occurs de novo.
Language	English
Publishing date	2018-06-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2672872-2
ISSN	2192-8312 ; 2192-8304
ISSN (online)	2192-8312
ISSN	2192-8304
DOI	10.1007/8904_2018_111
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Article ; Online: PTEN hamartoma tumor syndrome: an overview.

Hobert, Judith A / Eng, Charis

Genetics in medicine : official journal of the American College of Medical Genetics

2009 Volume 11, Issue 10, Page(s) 687–694

Abstract: PTEN hamartoma tumor syndrome (PHTS) encompasses four major clinically distinct syndromes associated with germline mutations in the tumor suppressor PTEN. These allelic disorders, Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and ... ...

Abstract	PTEN hamartoma tumor syndrome (PHTS) encompasses four major clinically distinct syndromes associated with germline mutations in the tumor suppressor PTEN. These allelic disorders, Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Proteus-like syndrome are associated with unregulated cellular proliferation leading to the formation of hamartomas. Thus far, an increased risk of malignancy has only been documented in Cowden syndrome; however, current recommendations advise that all individuals with PTEN hamartoma tumor syndrome follow the cancer surveillance strategies suggested for Cowden syndrome until further data indicate otherwise. Because any individual phenotypic feature of Cowden syndrome and Bannayan-Riley-Ruvalcaba syndrome are frequently present in the general population, many individuals often go undiagnosed and consequently do not benefit from available cancer surveillance strategies. Therefore, it is critical for clinicians to recognize the phenotypic features associated with these syndromes to accurately diagnose and provide preventative care. This overview details the clinical description of the PTEN hamartoma tumor syndrome and associated disorders, their diagnosis and molecular/genetic testing, as well as differential diagnosis for assessment of other hamartoma-associated syndromes.
MeSH term(s)	Diagnosis, Differential ; Genetic Counseling ; Hamartoma Syndrome, Multiple/complications ; Hamartoma Syndrome, Multiple/diagnosis ; Hamartoma Syndrome, Multiple/genetics ; Hamartoma Syndrome, Multiple/therapy ; Humans ; Molecular Diagnostic Techniques
Language	English
Publishing date	2009-08-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1455352-1
ISSN	1530-0366 ; 1098-3600
ISSN (online)	1530-0366
ISSN	1098-3600
DOI	10.1097/GIM.0b013e3181ac9aea
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Article: A novel role of the Batten disease gene CLN3: association with BMP synthesis.

Hobert, Judith A / Dawson, Glyn

Biochemical and biophysical research communications

2007 Volume 358, Issue 1, Page(s) 111–116

Abstract: Juvenile Neuronal Ceroid Lipofuscinosis (JNCL) results from a deficiency of CLN3, a protein recently identified within detergent-resistant membranes (DRMs). To study the function of CLN3 within these domains we isolated DRMs from control and JNCL-brain ... ...

Abstract	Juvenile Neuronal Ceroid Lipofuscinosis (JNCL) results from a deficiency of CLN3, a protein recently identified within detergent-resistant membranes (DRMs). To study the function of CLN3 within these domains we isolated DRMs from control and JNCL-brain and noted that JNCL-derived DRMs are less buoyant than control. Analysis of DRM phospholipids derived from JNCL-brain revealed a reduction of bis(monoacylglycerol)phosphate. Metabolic labeling of JNCL-fibroblasts demonstrated a reduction in the synthesis of bis(monoacylglycerol)phosphate which was restored following complementation with wild-type-CLN3, substantiating our initial observation in brain. Metabolic labeling of cell lines overexpressing wild-type-CLN3 resulted in increased bis(monoacylglycerol)phosphate synthesis, while overexpression of mutant CLN3-L170P decreased bis(monoacylglycerol)phosphate synthesis. These data illustrate a new finding, a strong correlation between CLN3 protein expression and synthesis of bis(monoacylglycerol)phosphate.
MeSH term(s)	Brain/metabolism ; Cells, Cultured ; Fibroblasts/metabolism ; Humans ; Intracellular Membranes/metabolism ; Lysophospholipids/biosynthesis ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Membrane Microdomains/metabolism ; Molecular Chaperones/genetics ; Molecular Chaperones/metabolism ; Monoglycerides/biosynthesis ; Mutation ; Neuronal Ceroid-Lipofuscinoses/metabolism
Chemical Substances	CLN3 protein, human ; Lysophospholipids ; Membrane Glycoproteins ; Molecular Chaperones ; Monoglycerides ; bis(monoacylglyceryl)phosphate
Language	English
Publishing date	2007-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2007.04.064
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Article: Neuronal ceroid lipofuscinoses therapeutic strategies: past, present and future.

Hobert, Judith A / Dawson, Glyn

Biochimica et biophysica acta

2006 Volume 1762, Issue 10, Page(s) 945–953

Abstract: Historically, many different therapies have been assessed for their ability to alter disease progression of the Neuronal Ceroid Lipofuscinoses (NCLs). While some treatments have lead to minor improvements, none have been able to arrest disease ... ...

Abstract	Historically, many different therapies have been assessed for their ability to alter disease progression of the Neuronal Ceroid Lipofuscinoses (NCLs). While some treatments have lead to minor improvements, none have been able to arrest disease progression or improve the quality or duration of life. Presently, many new therapeutic strategies, such as chaperone therapy, enzyme replacement therapy, gene therapy, and stem cell therapy, are being investigated for their ability to alter the disease course of the NCLs. This review summarizes previous studied therapies, discusses those currently being evaluated and examines possibilities for future therapies for the treatment of patients with NCL.
MeSH term(s)	Animals ; Clinical Trials as Topic ; Dietary Supplements ; Genetic Therapy ; Humans ; Lysosomes/enzymology ; Mice ; Molecular Chaperones/therapeutic use ; Neuronal Ceroid-Lipofuscinoses/enzymology ; Neuronal Ceroid-Lipofuscinoses/genetics ; Neuronal Ceroid-Lipofuscinoses/therapy ; Stem Cell Transplantation
Chemical Substances	Molecular Chaperones
Language	English
Publishing date	2006-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2006.08.004
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